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Modulatory effect of ursolic acid on neurodegenerative activities in oxidative brain injury: An ex vivo study
Journal of Food Biochemistry ( IF 3.5 ) Pub Date : 2020-12-23 , DOI: 10.1111/jfbc.13597
Veronica F Salau 1, 2 , Ochuko L Erukainure 1, 3 , Gideon Ayeni 4 , Collins U Ibeji 5 , Md Shahidul Islam 1
Affiliation  

Natural products‐based antioxidants have been well reported for their therapeutic benefits in the treatment and management of neurodegenerative diseases. The neuroprotective effect of ursolic acid (UA) against oxidative injury was investigated in isolated rat brain. Induction of oxidative injury in isolated rat brains with 0.1 mM FeSO4 led to depleted levels of glutathione, superoxide dismutase, catalase, and ENTPDase activities, with concomitant exacerbation of malondialdehyde and nitric oxide levels, α‐chymotrypsin, ATPase, and acetylcholinesterase activities. These levels and activities were significantly reversed following treatment of the brain tissues with UA. Molecular docking studies revealed strong molecular interactions between UA, catalase, and ATPase. Overall, these results indicate the neuroprotective effect of UA against oxidative injury in isolated rat brains as depicted by their ability to mitigate oxidative stress, purinergic, and cholinergic dysfunctions, with concomitant suppression of proteolytic activity.

中文翻译:


熊果酸对氧化性脑损伤中神经退行性活动的调节作用:一项离体研究



基于天然产物的抗氧化剂在神经退行性疾病的治疗和管理中的治疗效果已得到充分报道。在离体大鼠脑中研究了熊果酸(UA)对氧化损伤的神经保护作用。用 0.1 mM FeSO 4在离体大鼠脑中诱导氧化损伤,导致谷胱甘肽、超氧化物歧化酶、过氧化氢酶和 ENTPDase 活性水平下降,同时丙二醛和一氧化氮水平、α-胰凝乳蛋白酶、ATP 酶和乙酰胆碱酯酶活性加剧。用 UA 处理脑组织后,这些水平和活性显着逆转。分子对接研究揭示了 UA、过氧化氢酶和 ATP 酶之间强烈的分子相互作用。总体而言,这些结果表明 UA 对离体大鼠大脑中的氧化损伤具有神经保护作用,其减轻氧化应激、嘌呤能和胆碱能功能障碍的能力,同时抑制蛋白水解活性。
更新日期:2021-02-22
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